ArticleJournal of molecular neuroscience : MN2017
Mfn2-Mediated Preservation of Mitochondrial Function Contributes to the Protective Effects of BHAPI in Response to Ischemia.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Iron Overload Mediates the Differential Cell Fate of Astrocytes from Neurons and Its Regulatory Mechanisms in Ischemic Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Prediction of Post-Stroke Cognitive Impairment Based on Iron Metabolism Parameters: Results From A Prospective Study.Molecular neurobiology · 2025Article
- The Role of Mitochondrial Dynamin in Stroke.Oxidative medicine and cellular longevity · 2022Review
- Therapeutic effects of stem cells in different body systems, a novel method that is yet to gain trust: A comprehensive review.Bosnian journal of basic medical sciences · 2021Review
- Ironing Out the Details: How Iron Orchestrates Macrophage Polarization.Frontiers in immunology · 2021Review
- Stem Cells as Drug-like Biologics for Mitochondrial Repair in Stroke.Pharmaceutics · 2020Review
- Stroke gets in your eyes: stroke-induced retinal ischemia and the potential of stem cell therapy.Neural regeneration research · 2020Review
- Astragalus Polysaccharide Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Oxidative Damage and Mitochondrial Dysfunction.BioMed research international · 2020Article
- The brain and eye: Treating cerebral and retinal ischemia through mitochondrial transfer.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Eye Opener in Stroke.Stroke · 2019Article
- B355252, A Novel Small Molecule, Confers Neuroprotection Against Cobalt Chloride Toxicity In Mouse Hippocampal Cells Through Altering Mitochondrial Dynamics And Limiting Autophagy Induction.International journal of medical sciences · 2018Article
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Authors and funding
7 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Disturbances in intracellular iron homeostasis are associated with neuronal injury after stroke. However, exposure of cells to classical chelators may interfere with physiological iron functions. BHAPI is an iron prochelator that exerts strong iron binding capacity only under oxidative stress conditions. This study investigated the protective effects of N'-(1-(2-((4-(4,4,5,5-tetramethyl-1,2,3-dioxoborolan-2-yl)benzyl)oxy)phenyl)ethylidene (BHAPI) on an in vitro ischemia model mimicked by oxygen and glucose deprivation (OGD) in neuronal HT22 cells. The results showed that BHAPI significantly increased cell viability and decreased lactate dehydrogenase (LDH) release after OGD. BHAPI treatment also reduced apoptosis, as measured by flow cytometry, and suppressed caspase-3 activation. These protective effects were accompanied by preserved mitochondrial membrane potential (MMP), reduced mitochondrial swelling, promoted mitochondrial calcium buffering capacity, and increased mitochondrial respiration. The results of MitoTracker staining showed that BHAPI partially prevented the OGD-induced changes in mitochondrial morphology. Furthermore, BHAPI selectively increased the expression of mitochondrial dynamic protein Mfn2, with no effect on Mfn1 expression. Knockdown of Mfn2 with specific siRNA partially reversed the protective effects of BHAPI. In summary, the iron prochelator BHAPI protects HT22 cells against ischemic injury through preservation of mitochondrial function and Mfn2 signaling.
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